Arteriosclerotic lesions are found in the coronary arteries of spawning Pacific salmon (Oncorhynchus) and steelhead trout that survive the spawning act. Spawning and postspawning salmon have a profound abnormality in their blood coagulation mechanism which has been attributed to disseminated intravascular thrombosis or clotting (DIC). It is possible that the arterial lesions might represent small thrombi which become covered over by endothelial cells and then are incorporated into the intima. Focal necrotic lesions are found in the gills of these fish and it has been suggested that these are embolic in nature. Are these lesions and those in the coronary arteries related in any way to the coagulation abnormalities? Raising the temperature even a few degrees produces marked shortening of prothrombin and partial thromboplastin times in salmon and these findings are far more striking than any of the changes of "hypercoagulability" seen in women on the pill. Will "hypercoagulability" if defined as acceleration of the in vitro clotting time, predispose to thrombosis with or without arterial lesions? We hope to obtain answers to some of these questions by a careful gross, electron and light microscopic examination of the organs and tissues of spawning and post-spawning salmon, carefully searching for evidence of thromboembolic disease with particular attention to the lesions in the gills and the evolution of the arteriosclerotic lesions in the cornory arteries. Using the same techniques we will also study the lesions, if any, that occur in the "hypercoagulability" induced by raising the temperature in salmon and/or infusion of serum. If a relationship between "hypercoagulability" and areteriosclerosis is established, this would supply the first good experimental support to the old Rokitansky- Duguid encrustation theory of atherosclerosis.